Proteomic approaches to study epigallocatechin gallate-provoked apoptosis of TSGH-8301 human urinary bladder carcinoma cells: roles of AKT and heat shock protein 27-modulated intrinsic apoptotic pathways.

摘要: Epigallocatechin-3-gallate (EGCG), a polyphenol constituent present in green tea, has been shown to inhibit the growth of cancer cells in vitro and in vivo. However, studies regarding human bladder carcinoma are limited not well investigated. Hence, our study focused on evaluation EGCG-triggered apoptosis TSGH-8301 urinary in vivo as its related molecular mechanisms. In an study, EGCG inhibited xenograft tumor size nude mouse model. Based resulted morphological changes increased inhibition dose- time-dependent manner cells. Furthermore, sub-G1 populations were caspase-9 -3 activities stimulated EGCG-treated Moreover, inhibitor (Z-LEHD-FMK) caspase-3 (Z-DEVD-FMK) able reduce EGCG-stimulated activities, respectively. Loss mitochondrial membrane potential (∆Ψm) increase protein levels cytochrome c, Apaf-1, following exposure EGCG. Proteomic analysis revealed that affected expression various proteins, including HSP27, porin, tropomyosin 3 isoform 2, prohibitin keratin 5, 14, 17 also suppressed AKT kinase activity altered Bcl-2 family-related proteins such Bcl-2, Bax, BAD p-BAD. above findings, this suggests EGCG-provoked apoptotic death is mediated through targeting HSP27 modulating p-BAD, leading activation intrinsic pathway.